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Università di Verona                          AOUI di Verona
   Dipartimento di                         Istituto del Pancreas
     Medicina




                        L’eterogeneità
                       della pancreatite
                            cronica
                         Italo Vantini
Conoscere una malattia - 1
• La conoscenza delle connotazioni di una
  malattia consente di fornire:
   – una descrizione utile per l’inquadramento
     classificativo (nosologico) (che cosa è)
     •   Etiopatogenetica
     •   Clinica
     •   Anatomopatologica
     •   Fisiopatologica
  – un “nome”’per la sua identificazione
    nosologica (condivisione di come si chiama)
Conoscere una malattia - 2
• Una diagnosi
  – Matching, illness script, exemplars
  – Percorsi probabilistici
  – Criteri, strumenti, percorsi, processi
• La diagnosi non è “tanto” l’inserimento del
  paziente in una “casella nosologica, ma un
  giudizio basato su dati e criteri utili per
  assumere decisioni operative ai fini della:
     • Prognosi
     • Terapia
In principio…

Sarles H, Sarles JC, Camatte R, Muratore
    R, Gaini M, Guien C, Pastor J, Le Roy
                      F
Observations on 205 confirmed cases of acute

          Gut 1965; 6: 545-59.
Chronic pancreatitis
Chronic process characterized
  by inflammatory and fibrotic
   changes of the pancreas.
Irreversible nature of structural
   changes and progressive
     functional impairment
Chronic pancreatitis


                     Fibrosis of the pancreas
                     Damage to the acinar tissue
morphologically      Changes in ductal system
                  •   Calcifications
Chronic pancreatitis: progressive
    parenchymal changes

           Normal pancreas




          Moderate changes more or less
          scattered troughout the pancreas




            Advanced changes (fibrosis)
Chronic pancreatitis: pancreatic duct
Pancreatic calcification
Chronic pancreatitis
clinically   • Recurrent or
               persistent
               pancreatic pain
Pain in chronic pancreatitis
            Clinical pictures
     Type 1pain recurrent with lasting
                   pain-free intervals
     Type 2 pain : frequent, persisting,
                   disabling pain
              PATHOPHYSIOLOGY
               • Acute inflammation
                    • Ischemia
• Increased intraductal and parenchymal pressure
    • Mechanical compression (e.g. pseudocyst)
 Pancreatic neural remodelling and neuropathy
Chronic pancreatitis
                  • Recurrent or persistent
  clinically        pancreatic pain
                    Changes in ductal system
                  • Fibrosis of the pancreas
morphologically   • calcification


                  • Deterioration in
  functionally      pancreatic function
                    (exocrine and endocrine)
Frequency of painful relapses/year in 199
          patients with chronic pancreatitis
    (non-operated upon) followed up to 20 years
                 Prevention and               treatment                    percentiles
                                                                          Treatment of               25°
                    early
                    treatment                of advanced
                                                relapsing                exocrine failure
                                                                                    late
               of painful relapses        or persisting pain             and secondary               50°
             5 and complications
                                                                            diabetes                 75°
             4
N. painful
 relapses




                                                             in time
             3
                                                          on
                                                   sfuncti
                                            and dy
             2
                                          n
             1
                             Calcificatio
             0
                 1   2   3   4   5   6   7   8   9   10   11   12   13   14 15   16   17   18   19   20




                                                                                                          25°
                                         years since clinical onset

        Scuro LA et al , Am J Gastroenterol 1983; 78: 495-501.
        Ammann RW et al. Gastroenterology 1984, 86: 820-8..
alcool
Alcohol and chronic pancreatitis
                   - relative risk -
     16
     14
     12
     10
                                                        chronic
                                                        pancreatitis
OR    8
      6
                                                        cancer without CP
      4
      2
      0
           0-40          41-80           81- 240
                  grams of alcohol/day
                                              Durbec J, Sarles H: Digestion 1973
                                              Talamini G. et al Dig Dis Sci 1999
pain




function
Chronic Pancreatitis
                  (“old concepts”) - 1
 a single and distinct entity
 a well defined epidemiological
  and clinical pattern
    Male/female 4:1; age onset 47 year old
alcoholic in origin
 (in Western Countries)

 Differs from Acute Pancreatitis
(etiology, clinical outcome,prognosis)
    Acute and chronic pancreatitis are two distinct entities
Pancreatologia
    felix
Chronic Pancreatitis
                           Alcohol abuse in more recent studies
                100
                 90
                 80
% of patients




                 70
                 60
                 50
                40
                30
                20
                10
                 0
                       Italy 2009°         India 2008*          USA 2008^   China 2009"
                      893 pts                 1033 pts           540 pts    2008 pts

  °        Frulloni L et al, PanCroInfAISP, Dig Liv Dis 2009; 41: 311-317
  *        Balakrishnan V et al, J Pancreas, 2008; 9: 593-600
  ^        Withcomb DC et al, NAPS2, Pancreatol, 2008; 8: 520-531
  ”        Whang LW et al, Chinese CPSG, Pancreas, 2008; 38:248-54.
Smoking and chronic pancreatitis:
                         a meta-analysis




Andriulli A, Botteri E, Almasio PL, Vantini I, Uomo G, Maisonneuve P: Smoking as a
cofactor for causation of chronic pancreatitis. Pancreas 2010; 39: 1205- 1210
Smoking and pancreatic calcification



                                   Giving-up smoking within 5
                                years since onset of CP reduces
                                the risk of developing pancreatic
                                           calcifications

                                             Talamini G et al
                                         Pancreas. 2007 ;35:320-6.




Talamini G, Bassi C, Falconi M, Sartori N, Vaona B, Bovo P, Benini L, Cavallini G, Pederzoli P, Vantini I
Smoking cessation at the clinical onset of chronic pancreatitis and risk of pancreatic calcification.
Pancreatic acinar cell damage in response to cigarette smoke
 components : sensitization to acinar cell injury, that can be
             worsened by alcohol consumption

                                                                    similar
                Trypsinogen                                           to
                but not PSTI                                     experimental
                                                                    acute
                                                                  pancreatitis


                        Cytoplasmic
oxidative                 swelling
stress and
lipid
perossidation




                           Alexander M et al Pancreatology; 2011: 11: 469-74
L'eterogeneità della pancreatite cronica - Gastrolearning®
Chronic Pancreatitis
              (“concepts”) -2

 a single and distinct entity
alcohol and smoke interact as risk
factors
increased risk of pancreatic cancer


     a single clinical pattern, though
             evolving in time
Epidemiological and clinical features of
       chronic pancreatitis: the identikit
•   Males (80%)
•   45 year old at the clinical onset
•   Alcohol abusers (40-60%)
•   Smokers in (> 80%)
•   Pancreatic calcification (20% at onset)
•   Dilation/changes of pancreatic duct system
•   Painful relapses
•   Progressive pancreatic failure (exocrine and
    endocrine)
Chronic pancreatis
               principles of therapy-2
• Prevention of relapses
   – Alcohol withdrawal in an early stage
• Reduction in the risk of pancreatic calcifications
  and of the progression of the disease
   – Smoking withdrawal
• Reduction in the risk of pancreatic cancer (?)
   – Smoking withdrawal
• Treatment of relapses
   – Treatment of acute flares (starvation, IV fluids, analgesic
     drugs)
• Treatment of disabling and severe pain and/or of
  complications
   – Surgery (drainage or resection) (not “untimed”)
     associated with alcohol withdrawal
• Treatment of exocrine failure
Pancreatologia
  triumphans
a “new” pancreatitis ?

 men
 heavy alcohol drinkers
 heavy smokers
 calcification (90%)
 dilation of the pancreatic duct (80%)
 aggressive painful pancreatitis, often
 disabling (> 50%)
 vomiting, jaundice
- pathology: cystic and solid types -




  Cystic Type (75%)    Solid Type (25%)
EUS findings

                      Normal
        cyst         Duodenal
                       Wall




 Thickened
duodenal wall



      cyst
Cystic dystrophy of the duodenal wall
               The “groove” area

              Groove           C       Groove


                                   C    BD
                              D           W

                               P




D = duodenum             P = papilla of Vater
BD = common bile duct    W = Wirsung’s duct
C = cyst
CYSTIC DYSTROPHY OF DUODENAL WALL




                A bud of dorsal pancreas,
           associated to the Santorini's duct,
           entrapped within the duodenal wall
                  during organogenesis
Paraduodenal pancreatitis
    (cystic or solid duodenal dystrophy)

        almost all men
 almost all heavy alcohol abusers
       almost all smokers
       calcification (90%)
    disabling painful relapses
  vomiting, jaundice (at onset)
Main clinical features in different types of
                         chronic pancreatitis




Alcoholic


Hereditary

Paraduod.


Obstructive


Painless


AIP
Alcoholic pancreatitis and paraduodenal
           pancreatitis (PDP)
• PDP pancreatitis shares the same risk factors and
  similar epidemiological and clinical pattern of alcoholic
  pancreatitis
• Morphologically is a distinc form of CP
• PDP clinically behaves a severe clinical form of
  alcoholic pancreatitis

• Though alcohol withdrawal can induce some clinical
  improvement, more than 50% of the patients are
  eligible for surgery because of invalidating pain and/or
  duodenal obstruction

• It is probable that old series of patients formerly
  classified as alcoholic pancreatitis were in fact PDP
cysts of the duodenal wall and chronic pancreatitis




                                      Dilation of Wirsung


                                  Head calcifications
                     D   Groove
                          Zone




D = duodenal lumen
W=Wirsung’s duct
Chronic pancreatitis
       Classification of Marseille-Rome 1990
• Alcoholic pancreatitis
• Obstructive pancreatitis
• Hereditary and familial pancreatitis
• Idiopathic pancreatitis
   – juvenile
   – senile (may be painless)

• Inflammatory pancreatitis


                      Sarles H, Scand J Gastroenterol, 1989; 24: 641-2
Obstruction and chronic pancreatitis

• Several experimental data on different
  animal models show that chronic
  pancreatitis cannot develop, irrespective
  of the type of the experimental damage,
  without an obstruction of the duct system
• Periductal inflammation can lead,
  together with stellate cells activation, to
  periductal fibrosis that can induce
  changes in the pancreatic duct system
Necrosis-fibrosis mechanism in chronic pancreatitis




                       Kloeppel G. et al. Pancreas, 1993; 8: 659-670
Following an acute pancreatitis

  Chronic pancreatitis can be the
   consequence of a necrosis-
Acute pancreatitis 8 months before
    fibrosis change, leading to
  obstruction of pancreatic duct
system, and then to inflammatory
        and fibrotic changes.
                          Acute necrotizing
                        pancreatitisan acutelead of
                                     can attack to
                         chronic pancreatitis before
                               pancreatitis 6 months
Acute pancreatitis: frequency of chronicization




                                               (19/88=22%)


        Lankish PG et al., Am J Gastroenterol, 2009; 104: 2796-2805
Acute pancreatitis: frequency of relapses
        following the first episode
   (alcoholic vs. non-alcoholic pancreatitis)

                           40%

                 32%




                           15%
                 10%




          Lankish PG et al. Am J Gastroenterol, 2009; 104: 2796-2805
“obstructive”
                       pancreatitis
                             Factors (different from
                      slow-growing tumors) hampering
                          the pancreatic outflow can
                         trigger a process leading to
                            obstructive pancreatitis
   A “dysfunction” at the Oddi’s sphincter (SOD)
    can lead to chronic pancreatitis obstructive
 Oddi’s sphincter inflammation with altered outflow
         can “trigger” chronic pancreatitis
An obstacle to the pancreatic outflow can be associated with
 relapsing pancreatitis without evidence of ductal changes
Dilatazione duttale e singola calcificazione
                 ostruente



        dilatazione duttale      Ricorrenze
                                  dolorose


          calcificazione
            ostruente
Obstruction is the most frequent
associated factor in women (46%)
              DLD 1999; 41. 311-17
Main clinical features in different types of
                         chronic pancreatitis




Alcoholic


Hereditary

Paraduod.


Obstructive


Painless


AIP
Pain in chronic pancreatitis
           Clinical pictures
    Type 1pain recurrent with lasting
                  pain-free intervals
    Type 2 pain : frequent, persisting,
                  disabling pain

      PATHOPHYSIOLOGY OF PAIN IN
      “OBSTRUCTIVE PANCREATITIS”
    Increased intraductal-parenchymal
pressure caused by decreased drainage of
   pancreatic juice into the duodenum
                     •
Uncomplicate chronic pancreatitis
                         - Indication for surgery -




    The rationale of drainage surgery is a decompression within the
ductal system and reduction in pain in a substantiaòproprtion of patients
L'eterogeneità della pancreatite cronica - Gastrolearning®
Large stone in the duct




ERCP following sphincterotomy,
 ESW and fragment extraction
Surgery (pancreatojejunostomy) vs. endoscopy
       (sphincterotomy) in chronic pancreatitis



Djuna L Cahen et al

                      NEJM 2007; 356: 676-84


Djuna L Cahen et al




                                        but in 6/7 evaluable patients
                                        submitted to rescue surgery,
                                              it was uneffective
Who are the main clinical and morphological
  features of the patients with good results of
drainage surgery and poor after endotherapy ?


• Advanced chronic pancreatitis
    In advanced chronic pancreatitis
•          with symptoms and distal
    Distal obstruction
•        obstruction, drainage surgery
    Calcifications (> 90% of the cases)
            is superior to endoscopic
•   Severe, recurrent pain
                     therapy
•   Not too enlarged head of the
    pancreas
Who are the patients with chronic pancreatitis in which the
    endoscopic therapy seems to be more effective ?


 •   single distal obstruction
 •   single distal stone
 •   short duration of the disease
 •   more aggressive, repeated stenting strategy
      – Pancreatic sphincterotomy
      – Stricture dilation
      – Repeated stenting
      – Stone removal
Farnbacher et al Gastrointest Endosc 2002; 56: 501-59
Costamagna G et al Endoscopy 2006; 38: 254-59
Dumonceau JM et al ESGE guidelines- Endoscopy 2012, 44. 784-96
For treating uncomplicated chronic pancreatitis
 (aimed at relieving pain) ESGE recommends
   ESW/ERCP at the first-time interval option.
   The clinical response should be evaluated
                     at 6-8 weeks.
           If it is unsatisfactory the case
    should be discussed in a multidisciplinary
                         team.
     Surgical options should be considered,
  in particular in patients with a predicted poor
    outcome after endosopic therapy (RG B)
Candidate parameters for selecting patients for
      appropriate treatment and timing
               (a multidimensional approach)
•   Aethiology, natural history
•   Duration of the disease (stage)
•   Clinical features (pain type, complications) and QOL scores
•   Morphological assessment
     – Main pancreatic duct and secondary branches changes
     – Distal stenosis (main duct, Santorini)
     – “Dominant” duct stricture
     – Single or multiple obstructions-strictures
     – Upstream dilation (+/-)
     – Stone (single, distal, multiple)
     – Ductal scars (necrosi/fibrosis)        However, pain
                                        can persist also following
     – Complications                 effective treatment of stricture,
•   Technical aspects and aggressive strategy or it can subside also
                                            if the stricture is not disappeared
Pain treatment: appropriate patient selection


• A proper patient selection is of vital importance in the
  indication and in the outcome of treatment, in particular
  case of endoscopic and surgical therapy

• A more aggressive endoscopic strategy probably will
  give better results in properly selected patients

• Surgery should be timed and tailored to the clinical
  features and risk assessment, morphological pictures,
  and the best as possibile assessment about the
  presumptive origin of pain. Combination surgery should
  be considered
Chronic pancreatitis: ERCP




                      “Small duct”
                       pancreatitis
Langenbecjs Arch Surg 2003; 388: 132-9
Frequency of painful relapses/year in 199
          patients with chronic pancreatitis
    (non-operated upon) followed up to 20 years

                                         Endoscopy-Surgery
                                                                           percentiles                 25°
                    early
                   Endotherapy
                                              advanced
                                          Medical treatment
                                                                             Medical
                                                                                   late
                 Medical treatment                                          treatment                  50°
             5
                                                                                                       75°
             4
N. painful
 relapses




                                                             in time
             3
                                                          on
                                                   sfuncti
                                            and dy
             2
                                          n
             1
                             Calcificatio
             0
                 1   2   3   4   5   6   7    8   9   10   11    12   13   14 15   16   17   18   19   20




                                                                                                            25°
                                         years since clinical onset

        Scuro LA et al , Am J Gastroenterol 1983; 78: 495-501.
        Ammann RW et al. Gastroenterology 1984, 86: 820-8..
25 years ago…..

• Amman RW et al Gastroenterology 1986
   – in chronic pancreatiis early surgery is
     associated with a poor cinical outcome
   – the natural history of CP indicates that in
     almost 2/3 of the patients pain
     spontaneously subsides in long-term
     evolution
   – Commentary (Gastronterology 1986)
       • “The patient patient and the impatient
         surgeon”
Chronic pancreatitis
       Classification of Marseille-Rome 1990
• Alcoholic pancreatitis
• Hereditary and familial
  pancreatitis
• Idiopathic pancreatitis
   – juvenile
   – senile (may be painless)
• Obstructive pancreatitis
             Sarles H, Scand J Gastroenterol, 1989; 24: 641-2
• Inflammatory pancreatitis
Gene-mutation associated pancreatitis
          Cationic Trypsinogen – PRSS14,5
               R122H, N29I, A16V, R116C, E79K, R112C, D22G, K23R


          Pancreatic Secretory Trypsin Inhibitor
           (PSTI) – SPINK16,7
               N34S, P55S, M1T, L14P, -53C>T, IVS3+2T>C

          CFTR gene1-3
                        F508 (nel 50-70% dei casi), altre mutazioni
1
  N Engl J Med, 1998: 339; 645-2
2
  N Engl J Med, 1998; 339: 653-8
3
  Eur J Hum Genet, 2003; 11: 543-6
4
  Gut, 2002;50:271-2.
5
  Gut, 2002; 50:687-92
6
  J Med Genet, 2000; 37:67-9
7
  Gut, 2002; 50:675-81
Gene-mutation associated pancreatitis
     Main features of Hereditary Pancreatitis
 Hereditary-Familial
     one or more relatives of the same familial kindred
      affected, at different or at the same generation,
      No other risk factor of pancreatitis (complete work-up)

 Juvenile onset < 10 years (< 20 years)
 Recurrent episodes of mild pancreatitis
 Progression of pancreatic calcifications
 Slow progression toward pancreatic failure
 Survival rate comparable to that of the general
  population
Cumulative risk of cancer in patients with
        Hereditary Pancreatitis
        (smokers vs. non smokers)

                                        smokers




                                         non-smokers




                   Lowenfels AB et al JAMA 2001; 286:169-70
pancreatite associata a mutazione del
                CFTR




                                          Pancreatite associata a
                                        mutazione del gene SPINK 1
SPINK1
    Chronic pancreatitis associated with gene
                   mutation
SPINK1      Bull-eye sign        SPINK1              Bull-eye sign




                                                             non smokers
CFTR
                                                                smokers




                        Graziani R. et al. Abdominal Radiology, 2010; 115: 885-88
                            Frulloni L, et al. Pancreas. 2008:371-
Chronic pancreatitis
     Classification of Marseille-Rome 1990
• Alcoholic pancreatitis
• Hereditary and familial pancreatitis
• Idiopathic pancreatitis
  – juvenile
  – senile (may be painless)
• Obstructive pancreatitis
• Inflammatory pancreatitis
                Sarles H, Scand J Gastroenterol, 1989; 24: 641-2
CFTR Normale                             CFTR Normale
             86,7%                                    95,7%




                                        CFTR
   CFTR                              1 Mutazione
1 Mutazione
                                      5,3%
 13,3%                                              Controlli
                                  RR = 2,52
                                  RR = 2,52        600 pazienti
 Pancreatite Cronica Idiopatica
          60 pazienti
L'eterogeneità della pancreatite cronica - Gastrolearning®
SPINK1 Normale                  SPINK1 Normale
         77%                            99,65%



           SPINK1
           Mutato
            23%         SPINK1
                      1 Mutazione
                         0,35%

Pancreatite Cronica                  Controlli
                                    279 pazienti
    Giovanile
      96 pazienti
Chronic pancreatitis and gene mutations

• Mutation in PRSS1 is present in ¼ of patients
  with juvenile-type chronic pancreatitis
• Up to 30% of idiopathic pancreatitis have a
  mutation in the CFTR allele vs. 3-5% in the
  general population, though a single mutation
  alone cannot trigger pancreatitis
• 20-30% of Hereditary Pancreatitis do not have
  PRSS1 mutation
• Mutation in PRSS1 is found in 20% of subjects
  who do not have any sign of pancreatitis
  (carriers)
                            Rebours V et al DLD 2012; 44: 8-15
Pancreatite associata ad alterazioni geniche

         Esordio clinico = Pancreatite acuta

     SI (87%)                               NO (13%)
   Età all’esordio           p = 0.005        Età all’esordio
    28 ± 14 anni                                44 ± 18 aa
CFTR-S = 30 ± 14 anni
CFTR-S = 30 ± 14 anni                    Clinica all’esordio:
                                          Clinica all’esordio:
CFTR-D = 20 ± 12 anni
CFTR-D = 20 ± 12 anni                     Dolore aspecifico (6)
                                           Dolore aspecifico (6)
SPINK1 = 24 ± 14 anni
SPINK1 = 24 ± 14 anni                     Dispepsia (2)
                                           Dispepsia (2)
     p = 0.027
     p = 0.027                            Ittero (1)
                                           Ittero (1)
                                          Altra patologia (2)
                                           Altra patologia (2)
 STORIA NATURALE DELLA PANCREATITE              10 di 11 pazienti
                                                 10 di 11 pazienti
   ASSOCIATA A MUTAZIONI GENICHE                = PC all’esordio
           Giulia De Marchi                      = PC all’esordio
          Tesi di Laurea, 2011
Long time ago….


                            “Why should the
                          pancreas be the only
                            human organ not
                             involved by an
Ludovico Antonio Scuro
                         autoimmune process?”
     1924 – 1989
Autoimmune pancreatitis
• Described by H. Sarles in 1961 yet,
• More than 900 papers published (most since
  ’90s)
• Accounts for
   – 4-6 % of all the patients with chronic pancreatitis
     referring to a terziary centre and for
   – about 20-40 % of idiopathic chronic pancreatitis


• Its aethiology is still unknown
  antibodies: CA II, Lactoferrin, SPTI antibodies
  (against host antigens); genetics: association with
  haplotype DRB1 0405 DQB1 0401; Polymorfism of
  Cytotoxic Lymphocyte-associated antigen-4 49A
Autoimmune Pancreatitis
            Main Clinical Features


No drinker and no smoker patients
Frequent association with other
 autoimmune diseases
Asymptomatic jaundice at onset
 (particularly in focal type)
“Atypical” pancreatitis at onset
 (particularly in diffuse type)
AIP Type 1 (70-85%)     AIP Type 2 (15-30%)
Pathology Definition




                       Lympho-Plasmacytic          Idiopathic
                           Sclerosing             Duct-Centric
                          Pancreatitis            Pancreatitis
                            (LPSP)                   (IDCP)


                         IgG4+ (ICH) – GEL–    IgG4– (ICH) – GEL+
                       IgG4 systemic disease   Inflammatory Bowel
                                                      Disease
Clinic




                          Relapses YES            Relapses NO
                             Steroids               Steroids
From Zamboni G et al
                          Type 1




Autoimmune Pancreatitis is a chronic
            pancreatitis
    LP . periductal inflammation
     IgG4 positive plasmacells
  Duct desctruction and narrowing
          Storiform fibrosis
Granulocytic Epithelial Lesion – GEL –
Zamboni G et at, Vierchow Arch, 2004; 445:
                 552-563

                                             Type 2
Diffuse AIP
   Sausage-like      Irregular narrowing




           mild pancreatitis
swelling              Capsule-like rim
Narrowed and irregular duct in autoimmune
           chronic pancreatitis

                               Associated with
                               a clinical picture
Autoimmune pancreatitis
           Focal and mass forming
               Early arterial phase


   Focal




Mass forming                               jaundice


                           University of Verona: Dpt. of Radiology
Mass forming AIP



                             ry
                        a to
                    d
                  an
                 m

      The problem is not to confirm
histologically AIP, but to exclude cancer
     by US or EUS-guided biopsies
                          University of Verona: Dpt. of Radiology
Mass-forming AIP: response to steroid therapy




CT at admission       15 days after initiation of steroids
Pancreatite acuta lieve seguita
Reperto    da precoce ricorrenza lieve
di base     e persistenza di moderata
             elevazione degli enzimi



                   Dopo terapia
                    steroidea




01-2009




                        02-2009
L'eterogeneità della pancreatite cronica - Gastrolearning®
ICDC   Autoimmune pancreatitis type 1: cardinal
       diagnostic criteria and levels of reliability




                    Shimosegawa T et al, Pancreas, 2011: 40: 352-358
ICDC           Autoimmune pancreatitis type 2:
       cardinal diagnostic criteria and levels of reliability




                         Shimosegawa T et al, Pancreas, 2011: 40: 352-358
Tipi di pancreatite autoimmune
              dopo completo work-up (ICDC)




92 Pazienti
                               Tsukasa Ikeura et al 2013, submitted
Three types of AIP: overlaps among
        diagnostic features



                    AIP type 2
  AIP type 1


               AIP NOS
Phil A Hart et al: Long-term outcomes of autoimmune pancreatitis:
a multicentre, international analysis
Gut Online First, published on December 11, 2012 as 10.1136/gutjnl-2012-30361
                                                             Type 1
23 institutions        1064              ICDC
                                                              978
 10 countries         patients          criteria
                                                             Type 2
                                                               86




    *




                         Type 1
                          31%
 Relapse rate                          (> in   IgG4 –related sclerosing cholangitis)
                         Type 2
                          9%

 * retreatment with steroids was equally effective
Phil A Hart et al: Long-term outcomes of autoimmune
  pancreatitis:a multicentre, international analysis
   Gut Online First, published on December 11, 2012 as 10.1136/gutjnl-2012-30361
Chronic pancreatitis



               paraduodenal
               alcoholic
                                       AIP
geneti
  c                      obstructive
         idiopatic

              painless
                                             Eterogeneity
                                              and ovelap
Classificazioni della pancreatite cronica
•   Etiologia, clinica e morfologia (nosografica)
     – Marsiglia 1963
     – Cambridge, 1983
     – Marsiglia 1984
     – Marsiglia-Roma 1988
•   Per stadio di malattia (early, late, advanced)
     – Chari ST, Singer MV Scand J Gastroenterol 1994; 29: 949-60
•   Per fattori di rischio
     – TIGAR-O Etemad B, Whitcomb DC. Gastroenterology. 2001
•   Per approccio operativo-terapeutico
     – Cavallini G, 2000 (“classificazione di Verona”)
•   Per probabilità di diagnosi (clinica, imaging, funzione, istologia)
     – Zurich 1997
     – JAP 1997
•   Per combinazione di clinica, probabilità di diagnosi, stadiazione,
    severità + score
     – M-ANNEHEIM (Schneider A, Lohr JM, Singer MV. J Clin
        Gastroenterol 2007; 42: 101-119)
M-ANNHEIM
              classification of chronic pancreatits


   Risk                                                    Probabaility of
• EZIOLOGICO
   factors                                                 the diagnosis
                                        Classification by



                                                                             Clinical
              Severity                                                       features and
                                                                             stage
Schneider A, Löhr JM, Singer MV.The M-ANNHEIM classification of chronic pancreatitis: introduction of a unifying
classification system based on a review of previous classifications of the disease.J Gastroenterol. 2007; 42:101-19.
Chronic pancreatitis

         - classifications and operative needs -

• Nosographic classification
• Diagnostic matching with illness scripts,
  exemplars,categories

• Operative classification
• Operative diagnosis targeted to decisions

• Complexity/undefined aspets/variation in time
• Diagnosis (disease) reliability : defined, probable,
  possible, undefined
EBM
EBM
      Evidence Level (EL) of the literature
           information/source of the
                  statements
          40

          35

          30

          25
  % of the
           20
statements
          15

          10

           5

           0
                 1        2        3         4        5

          According to Oxford Centre for Evidence Based Medicine
EBM
     Recommendation strenght of the statements,
          and agreement (consensus) rate
              40

              35

              30

              25
    % of the
              20
   statements
              15

              10

               5

               0
                       A            B            C         D

            According to Oxford Centre for Evidence Based Medicine
 83% of the statements: agreement rate*> 80%
* Agreement rate: “strongly agree or with minor reserve”
In principio…

Sarles H, Sarles JC, Camatte R, Muratore
    R, Gaini M, Guien C, Pastor J, Le Roy
                      F
Observations on 205 confirmed cases of acute

          Gut 1965; 6: 545-59.
George Wirsung………Wirsung duct




                        1642
Padova: giardino dei semplici
        (botanic garden )
L'eterogeneità della pancreatite cronica - Gastrolearning®

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L'eterogeneità della pancreatite cronica - Gastrolearning®

  • 1. Università di Verona AOUI di Verona Dipartimento di Istituto del Pancreas Medicina L’eterogeneità della pancreatite cronica Italo Vantini
  • 2. Conoscere una malattia - 1 • La conoscenza delle connotazioni di una malattia consente di fornire: – una descrizione utile per l’inquadramento classificativo (nosologico) (che cosa è) • Etiopatogenetica • Clinica • Anatomopatologica • Fisiopatologica – un “nome”’per la sua identificazione nosologica (condivisione di come si chiama)
  • 3. Conoscere una malattia - 2 • Una diagnosi – Matching, illness script, exemplars – Percorsi probabilistici – Criteri, strumenti, percorsi, processi • La diagnosi non è “tanto” l’inserimento del paziente in una “casella nosologica, ma un giudizio basato su dati e criteri utili per assumere decisioni operative ai fini della: • Prognosi • Terapia
  • 4. In principio… Sarles H, Sarles JC, Camatte R, Muratore R, Gaini M, Guien C, Pastor J, Le Roy F Observations on 205 confirmed cases of acute Gut 1965; 6: 545-59.
  • 5. Chronic pancreatitis Chronic process characterized by inflammatory and fibrotic changes of the pancreas. Irreversible nature of structural changes and progressive functional impairment
  • 6. Chronic pancreatitis  Fibrosis of the pancreas  Damage to the acinar tissue morphologically  Changes in ductal system • Calcifications
  • 7. Chronic pancreatitis: progressive parenchymal changes Normal pancreas Moderate changes more or less scattered troughout the pancreas Advanced changes (fibrosis)
  • 10. Chronic pancreatitis clinically • Recurrent or persistent pancreatic pain
  • 11. Pain in chronic pancreatitis Clinical pictures Type 1pain recurrent with lasting pain-free intervals Type 2 pain : frequent, persisting, disabling pain PATHOPHYSIOLOGY • Acute inflammation • Ischemia • Increased intraductal and parenchymal pressure • Mechanical compression (e.g. pseudocyst) Pancreatic neural remodelling and neuropathy
  • 12. Chronic pancreatitis • Recurrent or persistent clinically pancreatic pain Changes in ductal system • Fibrosis of the pancreas morphologically • calcification • Deterioration in functionally pancreatic function (exocrine and endocrine)
  • 13. Frequency of painful relapses/year in 199 patients with chronic pancreatitis (non-operated upon) followed up to 20 years Prevention and treatment percentiles Treatment of 25° early treatment of advanced relapsing exocrine failure late of painful relapses or persisting pain and secondary 50° 5 and complications diabetes 75° 4 N. painful relapses in time 3 on sfuncti and dy 2 n 1 Calcificatio 0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 25° years since clinical onset Scuro LA et al , Am J Gastroenterol 1983; 78: 495-501. Ammann RW et al. Gastroenterology 1984, 86: 820-8..
  • 15. Alcohol and chronic pancreatitis - relative risk - 16 14 12 10 chronic pancreatitis OR 8 6 cancer without CP 4 2 0 0-40 41-80 81- 240 grams of alcohol/day Durbec J, Sarles H: Digestion 1973 Talamini G. et al Dig Dis Sci 1999
  • 17. Chronic Pancreatitis (“old concepts”) - 1  a single and distinct entity  a well defined epidemiological and clinical pattern  Male/female 4:1; age onset 47 year old alcoholic in origin (in Western Countries)  Differs from Acute Pancreatitis (etiology, clinical outcome,prognosis)  Acute and chronic pancreatitis are two distinct entities
  • 18. Pancreatologia felix
  • 19. Chronic Pancreatitis Alcohol abuse in more recent studies 100 90 80 % of patients 70 60 50 40 30 20 10 0 Italy 2009° India 2008* USA 2008^ China 2009" 893 pts 1033 pts 540 pts 2008 pts ° Frulloni L et al, PanCroInfAISP, Dig Liv Dis 2009; 41: 311-317 * Balakrishnan V et al, J Pancreas, 2008; 9: 593-600 ^ Withcomb DC et al, NAPS2, Pancreatol, 2008; 8: 520-531 ” Whang LW et al, Chinese CPSG, Pancreas, 2008; 38:248-54.
  • 20. Smoking and chronic pancreatitis: a meta-analysis Andriulli A, Botteri E, Almasio PL, Vantini I, Uomo G, Maisonneuve P: Smoking as a cofactor for causation of chronic pancreatitis. Pancreas 2010; 39: 1205- 1210
  • 21. Smoking and pancreatic calcification Giving-up smoking within 5 years since onset of CP reduces the risk of developing pancreatic calcifications Talamini G et al Pancreas. 2007 ;35:320-6. Talamini G, Bassi C, Falconi M, Sartori N, Vaona B, Bovo P, Benini L, Cavallini G, Pederzoli P, Vantini I Smoking cessation at the clinical onset of chronic pancreatitis and risk of pancreatic calcification.
  • 22. Pancreatic acinar cell damage in response to cigarette smoke components : sensitization to acinar cell injury, that can be worsened by alcohol consumption similar Trypsinogen to but not PSTI experimental acute pancreatitis Cytoplasmic oxidative swelling stress and lipid perossidation Alexander M et al Pancreatology; 2011: 11: 469-74
  • 24. Chronic Pancreatitis (“concepts”) -2  a single and distinct entity alcohol and smoke interact as risk factors increased risk of pancreatic cancer  a single clinical pattern, though evolving in time
  • 25. Epidemiological and clinical features of chronic pancreatitis: the identikit • Males (80%) • 45 year old at the clinical onset • Alcohol abusers (40-60%) • Smokers in (> 80%) • Pancreatic calcification (20% at onset) • Dilation/changes of pancreatic duct system • Painful relapses • Progressive pancreatic failure (exocrine and endocrine)
  • 26. Chronic pancreatis principles of therapy-2 • Prevention of relapses – Alcohol withdrawal in an early stage • Reduction in the risk of pancreatic calcifications and of the progression of the disease – Smoking withdrawal • Reduction in the risk of pancreatic cancer (?) – Smoking withdrawal • Treatment of relapses – Treatment of acute flares (starvation, IV fluids, analgesic drugs) • Treatment of disabling and severe pain and/or of complications – Surgery (drainage or resection) (not “untimed”) associated with alcohol withdrawal • Treatment of exocrine failure
  • 28. a “new” pancreatitis ?  men  heavy alcohol drinkers  heavy smokers  calcification (90%)  dilation of the pancreatic duct (80%)  aggressive painful pancreatitis, often disabling (> 50%)  vomiting, jaundice
  • 29. - pathology: cystic and solid types - Cystic Type (75%) Solid Type (25%)
  • 30. EUS findings Normal cyst Duodenal Wall Thickened duodenal wall cyst
  • 31. Cystic dystrophy of the duodenal wall The “groove” area Groove C Groove C BD D W P D = duodenum P = papilla of Vater BD = common bile duct W = Wirsung’s duct C = cyst
  • 32. CYSTIC DYSTROPHY OF DUODENAL WALL A bud of dorsal pancreas, associated to the Santorini's duct, entrapped within the duodenal wall during organogenesis
  • 33. Paraduodenal pancreatitis (cystic or solid duodenal dystrophy)  almost all men  almost all heavy alcohol abusers  almost all smokers  calcification (90%)  disabling painful relapses  vomiting, jaundice (at onset)
  • 34. Main clinical features in different types of chronic pancreatitis Alcoholic Hereditary Paraduod. Obstructive Painless AIP
  • 35. Alcoholic pancreatitis and paraduodenal pancreatitis (PDP) • PDP pancreatitis shares the same risk factors and similar epidemiological and clinical pattern of alcoholic pancreatitis • Morphologically is a distinc form of CP • PDP clinically behaves a severe clinical form of alcoholic pancreatitis • Though alcohol withdrawal can induce some clinical improvement, more than 50% of the patients are eligible for surgery because of invalidating pain and/or duodenal obstruction • It is probable that old series of patients formerly classified as alcoholic pancreatitis were in fact PDP
  • 36. cysts of the duodenal wall and chronic pancreatitis Dilation of Wirsung Head calcifications D Groove Zone D = duodenal lumen W=Wirsung’s duct
  • 37. Chronic pancreatitis Classification of Marseille-Rome 1990 • Alcoholic pancreatitis • Obstructive pancreatitis • Hereditary and familial pancreatitis • Idiopathic pancreatitis – juvenile – senile (may be painless) • Inflammatory pancreatitis Sarles H, Scand J Gastroenterol, 1989; 24: 641-2
  • 38. Obstruction and chronic pancreatitis • Several experimental data on different animal models show that chronic pancreatitis cannot develop, irrespective of the type of the experimental damage, without an obstruction of the duct system • Periductal inflammation can lead, together with stellate cells activation, to periductal fibrosis that can induce changes in the pancreatic duct system
  • 39. Necrosis-fibrosis mechanism in chronic pancreatitis Kloeppel G. et al. Pancreas, 1993; 8: 659-670
  • 40. Following an acute pancreatitis Chronic pancreatitis can be the consequence of a necrosis- Acute pancreatitis 8 months before fibrosis change, leading to obstruction of pancreatic duct system, and then to inflammatory and fibrotic changes. Acute necrotizing pancreatitisan acutelead of can attack to chronic pancreatitis before pancreatitis 6 months
  • 41. Acute pancreatitis: frequency of chronicization (19/88=22%) Lankish PG et al., Am J Gastroenterol, 2009; 104: 2796-2805
  • 42. Acute pancreatitis: frequency of relapses following the first episode (alcoholic vs. non-alcoholic pancreatitis) 40% 32% 15% 10% Lankish PG et al. Am J Gastroenterol, 2009; 104: 2796-2805
  • 43. “obstructive” pancreatitis Factors (different from slow-growing tumors) hampering the pancreatic outflow can trigger a process leading to obstructive pancreatitis A “dysfunction” at the Oddi’s sphincter (SOD) can lead to chronic pancreatitis obstructive Oddi’s sphincter inflammation with altered outflow can “trigger” chronic pancreatitis An obstacle to the pancreatic outflow can be associated with relapsing pancreatitis without evidence of ductal changes
  • 44. Dilatazione duttale e singola calcificazione ostruente dilatazione duttale Ricorrenze dolorose calcificazione ostruente
  • 45. Obstruction is the most frequent associated factor in women (46%) DLD 1999; 41. 311-17
  • 46. Main clinical features in different types of chronic pancreatitis Alcoholic Hereditary Paraduod. Obstructive Painless AIP
  • 47. Pain in chronic pancreatitis Clinical pictures Type 1pain recurrent with lasting pain-free intervals Type 2 pain : frequent, persisting, disabling pain PATHOPHYSIOLOGY OF PAIN IN “OBSTRUCTIVE PANCREATITIS” Increased intraductal-parenchymal pressure caused by decreased drainage of pancreatic juice into the duodenum •
  • 48. Uncomplicate chronic pancreatitis - Indication for surgery - The rationale of drainage surgery is a decompression within the ductal system and reduction in pain in a substantiaòproprtion of patients
  • 50. Large stone in the duct ERCP following sphincterotomy, ESW and fragment extraction
  • 51. Surgery (pancreatojejunostomy) vs. endoscopy (sphincterotomy) in chronic pancreatitis Djuna L Cahen et al NEJM 2007; 356: 676-84 Djuna L Cahen et al but in 6/7 evaluable patients submitted to rescue surgery, it was uneffective
  • 52. Who are the main clinical and morphological features of the patients with good results of drainage surgery and poor after endotherapy ? • Advanced chronic pancreatitis In advanced chronic pancreatitis • with symptoms and distal Distal obstruction • obstruction, drainage surgery Calcifications (> 90% of the cases) is superior to endoscopic • Severe, recurrent pain therapy • Not too enlarged head of the pancreas
  • 53. Who are the patients with chronic pancreatitis in which the endoscopic therapy seems to be more effective ? • single distal obstruction • single distal stone • short duration of the disease • more aggressive, repeated stenting strategy – Pancreatic sphincterotomy – Stricture dilation – Repeated stenting – Stone removal Farnbacher et al Gastrointest Endosc 2002; 56: 501-59 Costamagna G et al Endoscopy 2006; 38: 254-59 Dumonceau JM et al ESGE guidelines- Endoscopy 2012, 44. 784-96
  • 54. For treating uncomplicated chronic pancreatitis (aimed at relieving pain) ESGE recommends ESW/ERCP at the first-time interval option. The clinical response should be evaluated at 6-8 weeks. If it is unsatisfactory the case should be discussed in a multidisciplinary team. Surgical options should be considered, in particular in patients with a predicted poor outcome after endosopic therapy (RG B)
  • 55. Candidate parameters for selecting patients for appropriate treatment and timing (a multidimensional approach) • Aethiology, natural history • Duration of the disease (stage) • Clinical features (pain type, complications) and QOL scores • Morphological assessment – Main pancreatic duct and secondary branches changes – Distal stenosis (main duct, Santorini) – “Dominant” duct stricture – Single or multiple obstructions-strictures – Upstream dilation (+/-) – Stone (single, distal, multiple) – Ductal scars (necrosi/fibrosis) However, pain can persist also following – Complications effective treatment of stricture, • Technical aspects and aggressive strategy or it can subside also if the stricture is not disappeared
  • 56. Pain treatment: appropriate patient selection • A proper patient selection is of vital importance in the indication and in the outcome of treatment, in particular case of endoscopic and surgical therapy • A more aggressive endoscopic strategy probably will give better results in properly selected patients • Surgery should be timed and tailored to the clinical features and risk assessment, morphological pictures, and the best as possibile assessment about the presumptive origin of pain. Combination surgery should be considered
  • 57. Chronic pancreatitis: ERCP “Small duct” pancreatitis
  • 58. Langenbecjs Arch Surg 2003; 388: 132-9
  • 59. Frequency of painful relapses/year in 199 patients with chronic pancreatitis (non-operated upon) followed up to 20 years Endoscopy-Surgery percentiles 25° early Endotherapy advanced Medical treatment Medical late Medical treatment treatment 50° 5 75° 4 N. painful relapses in time 3 on sfuncti and dy 2 n 1 Calcificatio 0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 25° years since clinical onset Scuro LA et al , Am J Gastroenterol 1983; 78: 495-501. Ammann RW et al. Gastroenterology 1984, 86: 820-8..
  • 60. 25 years ago….. • Amman RW et al Gastroenterology 1986 – in chronic pancreatiis early surgery is associated with a poor cinical outcome – the natural history of CP indicates that in almost 2/3 of the patients pain spontaneously subsides in long-term evolution – Commentary (Gastronterology 1986) • “The patient patient and the impatient surgeon”
  • 61. Chronic pancreatitis Classification of Marseille-Rome 1990 • Alcoholic pancreatitis • Hereditary and familial pancreatitis • Idiopathic pancreatitis – juvenile – senile (may be painless) • Obstructive pancreatitis Sarles H, Scand J Gastroenterol, 1989; 24: 641-2 • Inflammatory pancreatitis
  • 62. Gene-mutation associated pancreatitis  Cationic Trypsinogen – PRSS14,5  R122H, N29I, A16V, R116C, E79K, R112C, D22G, K23R  Pancreatic Secretory Trypsin Inhibitor (PSTI) – SPINK16,7  N34S, P55S, M1T, L14P, -53C>T, IVS3+2T>C  CFTR gene1-3 F508 (nel 50-70% dei casi), altre mutazioni 1 N Engl J Med, 1998: 339; 645-2 2 N Engl J Med, 1998; 339: 653-8 3 Eur J Hum Genet, 2003; 11: 543-6 4 Gut, 2002;50:271-2. 5 Gut, 2002; 50:687-92 6 J Med Genet, 2000; 37:67-9 7 Gut, 2002; 50:675-81
  • 63. Gene-mutation associated pancreatitis Main features of Hereditary Pancreatitis  Hereditary-Familial one or more relatives of the same familial kindred affected, at different or at the same generation,  No other risk factor of pancreatitis (complete work-up)  Juvenile onset < 10 years (< 20 years)  Recurrent episodes of mild pancreatitis  Progression of pancreatic calcifications  Slow progression toward pancreatic failure  Survival rate comparable to that of the general population
  • 64. Cumulative risk of cancer in patients with Hereditary Pancreatitis (smokers vs. non smokers) smokers non-smokers Lowenfels AB et al JAMA 2001; 286:169-70
  • 65. pancreatite associata a mutazione del CFTR Pancreatite associata a mutazione del gene SPINK 1
  • 66. SPINK1 Chronic pancreatitis associated with gene mutation SPINK1 Bull-eye sign SPINK1 Bull-eye sign non smokers CFTR smokers Graziani R. et al. Abdominal Radiology, 2010; 115: 885-88 Frulloni L, et al. Pancreas. 2008:371-
  • 67. Chronic pancreatitis Classification of Marseille-Rome 1990 • Alcoholic pancreatitis • Hereditary and familial pancreatitis • Idiopathic pancreatitis – juvenile – senile (may be painless) • Obstructive pancreatitis • Inflammatory pancreatitis Sarles H, Scand J Gastroenterol, 1989; 24: 641-2
  • 68. CFTR Normale CFTR Normale 86,7% 95,7% CFTR CFTR 1 Mutazione 1 Mutazione 5,3% 13,3% Controlli RR = 2,52 RR = 2,52 600 pazienti Pancreatite Cronica Idiopatica 60 pazienti
  • 70. SPINK1 Normale SPINK1 Normale 77% 99,65% SPINK1 Mutato 23% SPINK1 1 Mutazione 0,35% Pancreatite Cronica Controlli 279 pazienti Giovanile 96 pazienti
  • 71. Chronic pancreatitis and gene mutations • Mutation in PRSS1 is present in ¼ of patients with juvenile-type chronic pancreatitis • Up to 30% of idiopathic pancreatitis have a mutation in the CFTR allele vs. 3-5% in the general population, though a single mutation alone cannot trigger pancreatitis • 20-30% of Hereditary Pancreatitis do not have PRSS1 mutation • Mutation in PRSS1 is found in 20% of subjects who do not have any sign of pancreatitis (carriers) Rebours V et al DLD 2012; 44: 8-15
  • 72. Pancreatite associata ad alterazioni geniche Esordio clinico = Pancreatite acuta SI (87%) NO (13%) Età all’esordio p = 0.005 Età all’esordio 28 ± 14 anni 44 ± 18 aa CFTR-S = 30 ± 14 anni CFTR-S = 30 ± 14 anni Clinica all’esordio: Clinica all’esordio: CFTR-D = 20 ± 12 anni CFTR-D = 20 ± 12 anni  Dolore aspecifico (6)  Dolore aspecifico (6) SPINK1 = 24 ± 14 anni SPINK1 = 24 ± 14 anni  Dispepsia (2)  Dispepsia (2) p = 0.027 p = 0.027  Ittero (1)  Ittero (1)  Altra patologia (2)  Altra patologia (2) STORIA NATURALE DELLA PANCREATITE 10 di 11 pazienti 10 di 11 pazienti ASSOCIATA A MUTAZIONI GENICHE = PC all’esordio Giulia De Marchi = PC all’esordio Tesi di Laurea, 2011
  • 73. Long time ago…. “Why should the pancreas be the only human organ not involved by an Ludovico Antonio Scuro autoimmune process?” 1924 – 1989
  • 74. Autoimmune pancreatitis • Described by H. Sarles in 1961 yet, • More than 900 papers published (most since ’90s) • Accounts for – 4-6 % of all the patients with chronic pancreatitis referring to a terziary centre and for – about 20-40 % of idiopathic chronic pancreatitis • Its aethiology is still unknown antibodies: CA II, Lactoferrin, SPTI antibodies (against host antigens); genetics: association with haplotype DRB1 0405 DQB1 0401; Polymorfism of Cytotoxic Lymphocyte-associated antigen-4 49A
  • 75. Autoimmune Pancreatitis Main Clinical Features No drinker and no smoker patients Frequent association with other autoimmune diseases Asymptomatic jaundice at onset (particularly in focal type) “Atypical” pancreatitis at onset (particularly in diffuse type)
  • 76. AIP Type 1 (70-85%) AIP Type 2 (15-30%) Pathology Definition Lympho-Plasmacytic Idiopathic Sclerosing Duct-Centric Pancreatitis Pancreatitis (LPSP) (IDCP) IgG4+ (ICH) – GEL– IgG4– (ICH) – GEL+ IgG4 systemic disease Inflammatory Bowel Disease Clinic Relapses YES Relapses NO Steroids Steroids
  • 77. From Zamboni G et al Type 1 Autoimmune Pancreatitis is a chronic pancreatitis LP . periductal inflammation IgG4 positive plasmacells Duct desctruction and narrowing Storiform fibrosis
  • 78. Granulocytic Epithelial Lesion – GEL – Zamboni G et at, Vierchow Arch, 2004; 445: 552-563 Type 2
  • 79. Diffuse AIP Sausage-like Irregular narrowing mild pancreatitis swelling Capsule-like rim
  • 80. Narrowed and irregular duct in autoimmune chronic pancreatitis Associated with a clinical picture
  • 81. Autoimmune pancreatitis Focal and mass forming Early arterial phase Focal Mass forming jaundice University of Verona: Dpt. of Radiology
  • 82. Mass forming AIP ry a to d an m The problem is not to confirm histologically AIP, but to exclude cancer by US or EUS-guided biopsies University of Verona: Dpt. of Radiology
  • 83. Mass-forming AIP: response to steroid therapy CT at admission 15 days after initiation of steroids
  • 84. Pancreatite acuta lieve seguita Reperto da precoce ricorrenza lieve di base e persistenza di moderata elevazione degli enzimi Dopo terapia steroidea 01-2009 02-2009
  • 86. ICDC Autoimmune pancreatitis type 1: cardinal diagnostic criteria and levels of reliability Shimosegawa T et al, Pancreas, 2011: 40: 352-358
  • 87. ICDC Autoimmune pancreatitis type 2: cardinal diagnostic criteria and levels of reliability Shimosegawa T et al, Pancreas, 2011: 40: 352-358
  • 88. Tipi di pancreatite autoimmune dopo completo work-up (ICDC) 92 Pazienti Tsukasa Ikeura et al 2013, submitted
  • 89. Three types of AIP: overlaps among diagnostic features AIP type 2 AIP type 1 AIP NOS
  • 90. Phil A Hart et al: Long-term outcomes of autoimmune pancreatitis: a multicentre, international analysis Gut Online First, published on December 11, 2012 as 10.1136/gutjnl-2012-30361 Type 1 23 institutions 1064 ICDC 978 10 countries patients criteria Type 2 86 * Type 1 31% Relapse rate (> in IgG4 –related sclerosing cholangitis) Type 2 9% * retreatment with steroids was equally effective
  • 91. Phil A Hart et al: Long-term outcomes of autoimmune pancreatitis:a multicentre, international analysis Gut Online First, published on December 11, 2012 as 10.1136/gutjnl-2012-30361
  • 92. Chronic pancreatitis paraduodenal alcoholic AIP geneti c obstructive idiopatic painless Eterogeneity and ovelap
  • 93. Classificazioni della pancreatite cronica • Etiologia, clinica e morfologia (nosografica) – Marsiglia 1963 – Cambridge, 1983 – Marsiglia 1984 – Marsiglia-Roma 1988 • Per stadio di malattia (early, late, advanced) – Chari ST, Singer MV Scand J Gastroenterol 1994; 29: 949-60 • Per fattori di rischio – TIGAR-O Etemad B, Whitcomb DC. Gastroenterology. 2001 • Per approccio operativo-terapeutico – Cavallini G, 2000 (“classificazione di Verona”) • Per probabilità di diagnosi (clinica, imaging, funzione, istologia) – Zurich 1997 – JAP 1997 • Per combinazione di clinica, probabilità di diagnosi, stadiazione, severità + score – M-ANNEHEIM (Schneider A, Lohr JM, Singer MV. J Clin Gastroenterol 2007; 42: 101-119)
  • 94. M-ANNHEIM classification of chronic pancreatits Risk Probabaility of • EZIOLOGICO factors the diagnosis Classification by Clinical Severity features and stage Schneider A, Löhr JM, Singer MV.The M-ANNHEIM classification of chronic pancreatitis: introduction of a unifying classification system based on a review of previous classifications of the disease.J Gastroenterol. 2007; 42:101-19.
  • 95. Chronic pancreatitis - classifications and operative needs - • Nosographic classification • Diagnostic matching with illness scripts, exemplars,categories • Operative classification • Operative diagnosis targeted to decisions • Complexity/undefined aspets/variation in time • Diagnosis (disease) reliability : defined, probable, possible, undefined
  • 96. EBM
  • 97. EBM Evidence Level (EL) of the literature information/source of the statements 40 35 30 25 % of the 20 statements 15 10 5 0 1 2 3 4 5 According to Oxford Centre for Evidence Based Medicine
  • 98. EBM Recommendation strenght of the statements, and agreement (consensus) rate 40 35 30 25 % of the 20 statements 15 10 5 0 A B C D According to Oxford Centre for Evidence Based Medicine 83% of the statements: agreement rate*> 80% * Agreement rate: “strongly agree or with minor reserve”
  • 99. In principio… Sarles H, Sarles JC, Camatte R, Muratore R, Gaini M, Guien C, Pastor J, Le Roy F Observations on 205 confirmed cases of acute Gut 1965; 6: 545-59.
  • 101. Padova: giardino dei semplici (botanic garden )

Notas del editor

  1. And the main but now old concepts were that cronic pancreatitis is (leggi)
  2. And the main but now old concepts were that cronic pancreatitis is (leggi)
  3. Pathologists told has that there is a particular type of pancreatitis arise from the duodenal wall. In duodenal wall there are islet of pancreas normally. In patients who drank a lot, this islet became inflammed inside the duodenal wall and later may grow and extend toward
  4. cresci
  5. Pathologists, first of all prof. Kloppel, teach us that in autoimmune pancreatitis the histologic findings are typical for the disease. We can see inflammatory infiltration in to the pancreas, mainly around the ducts, with rupture of the basal membrane and secondary destruction of pancreatic ducts.
  6. … . like in this case, presents an enlargement of the pancreatic head, but without any sign of vascular or soft tissue infiltration. This was the first control. Once the diagnosis is suspected, the second examination, ..
  7. Felicetti